Macrophage MHC receptor 2: A novel receptor on allograft (H-2DdKd)-induced macrophage (H-2DbKb) recognizing an MHC class I molecule, H-2Kd, in mice

Tashiro-Yamaji, Junko; Kubota, Takeshi; Yoshida, Ryotaro

doi:10.1016/j.gene.2006.07.004

Cited by 19 publications

(31 citation statements)

References 26 publications

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“…6). This K d value was similar to that (2.7 × 10 − 9 M) of the H-2K d molecule for mouse MMR2 (Tashiro-Yamaji et al, 2006b). R12 mAb is a mAb specific for mouse MMR2 (Tashiro-Yamaji et al, 2006b); and the amino-acid sequence of the MHC-binding site of mouse MMR2 was highly conserved with that of human MMR2 (Fig.…”

Section: Specific Binding Of Hla-b62 Pentamer To Human Mmr2 and Compesupporting

confidence: 68%

“…Unexpectedly, however, the ligand specificity of MMR2 on mouse AIM is very specific: the MMR2 is reactive toward H-2K d molecules with a K d value of 2.7 × 10 − 9 M; whereas the receptor does not react with other MHC class I molecules such as H-2D d , H-2D b , H-2D k , H-2K b , H-2K k , and H-2L d (Tashiro-Yamaji et al, 2006b). Similarly, the results of the BLAST search indicated that the amino-acid sequence of HLA-B62 showed 93.5% identity to that of HLA-B7; whereas HEK293T cells expressing human MMR2 reacted with HLA-B62, but not with HLA-B7 (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…When an appropriate primer set specific for mouse MMR2 cDNA was employed, a clear but small amount of PCR product of approximately 2-kb was obtained from the AIM RNA, but not from those of the other infiltrating cells (Tashiro-Yamaji et al, 2006b). In the present study, we unexpectedly found that PBMCs or monocytes, but not lymphocytes or granulocytes, from healthy volunteers who had never been allografted clearly expressed human MMR2 (Figs.…”

Section: Discussionmentioning

confidence: 99%

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HLA-B62 as a possible ligand for the human homologue of mouse macrophage MHC receptor 2 (MMR2) on monocytes

Shimizu¹,

Tashiro-Yamaji²,

Hayashi³

et al. 2010

Gene

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Section: Specific Binding Of Hla-b62 Pentamer To Human Mmr2 and Compesupporting

confidence: 68%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

HLA-B62 as a possible ligand for the human homologue of mouse macrophage MHC receptor 2 (MMR2) on monocytes

Shimizu¹,

Tashiro-Yamaji²,

Hayashi³

et al. 2010

Gene

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“…Although CTL-resistant allogeneic tissue (e.g., skin) or tumor cells (e.g., Meth A fibrosarcoma cells) were rejected with kinetics of clearance similar to those of allogeneic CTL-susceptible targets, allograft-induced macrophages (AIM) were the major effector cells responsible for the rejection (8,9). The infiltration of AIM preceded the infiltration of CTLs by several days during the course of allograft rejection (16 (27,28). These results indicate that two distinct populations of unique cytotoxic cells (i.e., CTLs and AIM) are induced in the allograft rejection site and that the infiltration of AIM responsible for rejection precedes that of the CTLs perforin-or FasL-dependently cytotoxic against cells expressing donor-related alloantigens.…”

Section: Discussionmentioning

confidence: 99%

Acute Rejection of Allografted CTL-Susceptible Leukemia Cells from Perforin/Fas Ligand Double-Deficient Mice

Nomi

Tashiro-Yamaji

Yamamoto

et al. 2007

The Journal of Immunology

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The generation of knockout mice demonstrated that CD4+, but not CD8+, T cells were essential for the rejection of allografted skin or heart, presumably because these targets were CTL resistant. In the case of CTL-susceptible targets (e.g., P815 mastocytoma cells and EL-4 or RLmale1 T lymphoma cells), however, it is assumed that the CTL is the effector cell responsible for allograft rejection and that perforin and Fas ligand (FasL) pathways are the killing mechanisms. In the present study, we examined the role of these cytotoxic molecules in the rejection of i.p. allografted CTL-susceptible leukemia cells. Unexpectedly, the allografted leukemia cells were acutely rejected from gld (a mutation of FasL), perforin−/−, or double-deficient mice. The peritoneal exudate cells from gld or normal mice showed T cell-, TCRαβ-, and perforin-dependent cytotoxic activity against the allograft, whereas the exudate cells from perforin−/− mice exhibited almost full cytotoxic activity in the presence of Fas-Fc. Furthermore, the infiltrates from double-deficient mice showed a high cytotoxic activity against the allografted cells even in the presence of anti-TCRαβ Ab or in the absence of T cells. The cytotoxic cells appeared to be macrophages, because they were Mac-1+ mononuclear cells with a kidney- or horseshoe-shaped nucleus and because the cytotoxic activity was completely suppressed by the addition of NG-monomethyl-l-arginine, an inhibitor of inducible NO synthase. These results indicate that macrophages are ready and available to kill CTL-susceptible allografts when CTLs lack both perforin and FasL molecules.

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“…Receptors have been found that are specific for H-2 molecules [12,13]. These macrophage MHC receptors (MMR) are important in the rejection of allogeneic skin grafts, but not lymphoma cells.…”

Section: Monocytes and Macrophagesmentioning

confidence: 99%

Innate immune cells in transplantation

Spahn¹,

Li²,

Kreisel

2014

Current Opinion in Organ Transplantation

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Purpose of review This review examines the recent literature on the role of innate cells in immunity to transplanted tissue. It specifically addresses the impact of monocytes/macrophages, neutrophils, NK cells, and platelets. Recent findings Current research indicates that innate immunity plays a dual role in response to transplanted tissue with the ability to either facilitate rejection or promote tolerance. Intriguingly, some of these cells are even capable of reacting to allogeneic cells, a feature usually only attributed to cells of the adaptive immune system. Summary This review highlights new therapeutic targets in the innate immune system that may be useful in the treatment of transplant recipients. It also emphasizes the need to use caution in exploring these new therapeutics.

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Macrophage MHC receptor 2: A novel receptor on allograft (H-2DdKd)-induced macrophage (H-2DbKb) recognizing an MHC class I molecule, H-2Kd, in mice

Cited by 19 publications

References 26 publications

HLA-B62 as a possible ligand for the human homologue of mouse macrophage MHC receptor 2 (MMR2) on monocytes

HLA-B62 as a possible ligand for the human homologue of mouse macrophage MHC receptor 2 (MMR2) on monocytes

Acute Rejection of Allografted CTL-Susceptible Leukemia Cells from Perforin/Fas Ligand Double-Deficient Mice

Innate immune cells in transplantation

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